Contralateral suppression of distortion‐product otoacoustic emissions declines with age: A comparison of findings in CBA mice with human listeners

Jacobson, Michael J.; Kim, Sunghee; Romney, Joshua; Liu, Hanjun; Frisina, Robert D.

doi:10.1097/00005537-200310000-00009

Cited by 87 publications

(74 citation statements)

References 54 publications

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“…Furthermore, it was shown that CBA mice, the widely accepted model of late-onset ARHL, showed better contralateral suppression of DPOAEs in young adults compared with the C57 early-onset ARHL strain. In terms of MOC efficacy in different parts of the cochlea, a stronger MOC effect in the low-and mid-frequency areas compared with the high-frequency area has been shown in other studies (Jacobson et al, 2003;Kim and Frisina, 2002). In this study, we could find that the morphological and functional phenotypes of C57 mice indicate that as compared to the CBA mice, C57 mice show greater dysfunction of the MOC efferent system as evidenced by abnormal morphology of the efferent OHC synapse.…”

Section: Discussionsupporting

confidence: 68%

Alpha-synuclein deficiency and efferent nerve degeneration in the mouse cochlea: A possible cause of early-onset presbycusis

Park

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Choung

et al. 2011

Neuroscience Research

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Section: Discussionsupporting

confidence: 68%

Alpha-synuclein deficiency and efferent nerve degeneration in the mouse cochlea: A possible cause of early-onset presbycusis

Park

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Choung

et al. 2011

Neuroscience Research

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“…This suggests that deafferentation following noise damage predominantly affects high-threshold AN fibers, while sufficient numbers of low-threshold AN fibers remain responsive to sound. Normal hearing thresholds can also be accompanied by impaired function of efferent fibers that project from the brainstem to the cochlea (Kim et al, 2002;Jacobson et al, 2003;Zettel et al, 2007;Zhu et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Tinnitus with a Normal Audiogram: Physiological Evidence for Hidden Hearing Loss and Computational Model

2011

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Ever since Pliny the Elder coined the term tinnitus, the perception of sound in the absence of an external sound source has remained enigmatic. Traditional theories assume that tinnitus is triggered by cochlear damage, but many tinnitus patients present with a normal audiogram, i.e., with no direct signs of cochlear damage. Here, we report that in human subjects with tinnitus and a normal audiogram, auditory brainstem responses show a significantly reduced amplitude of the wave I potential (generated by primary auditory nerve fibers) but normal amplitudes of the more centrally generated wave V. This provides direct physiological evidence of "hidden hearing loss" that manifests as reduced neural output from the cochlea, and consequent renormalization of neuronal response magnitude within the brainstem. Employing an established computational model, we demonstrate how tinnitus could arise from a homeostatic response of neurons in the central auditory system to reduced auditory nerve input in the absence of elevated hearing thresholds.

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“…Activation of this pathway ultimately leads to inhibition of the outer hair cell activity, and inhibition of DPOAE signals. A note on terminology: the modulation of DPOAE by the MOCS is commonly referred to as 'suppression' when it results in a reduction in DPOAE level [Abdala, 2001;James et al, 2002;Jacobson et al, 2003;James et al, 2005;James, 2011]. Considering that the MOCS can both suppress and enhance DPOAE, the effects are sometimes referred to as 'modulations' [Harrison et al, 2008].…”

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confidence: 99%

Separating the Contributions of Olivocochlear and Middle Ear Muscle Reflexes in Modulation of Distortion Product Otoacoustic Emission Levels

2013

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Objectives: Mediated by the medial olivocochlear system (MOCS), distortion product otoacoustic emission (DPOAE) levels are reduced by presentation of contralateral acoustic stimuli. Such acoustic signals can also evoke a middle ear muscle reflex (MEMR) that also attenuates recorded DPOAE levels. Our aim is to clearly differentiate these two inhibitory mechanisms and to analyze each separately, perhaps allowing the development of novel tests of hearing function. Methods: DPOAE were recorded in real time from chinchillas with normal auditory brainstem response thresholds and middle ear function. Amplitude reduction and its onset latency caused by contralateral presentation of intermittent narrow-band noise (NBN) were measured. Stapedius and tensor tympani muscle tendons were divided without disturbing the ossicular chain, and DPOAE testing was repeated. Results: Peak reduction of (2f₁ - f₂) DPOAE levels occurred when the center frequency of contralateral NBN approximated the primary tone f₂, indicating an f₂-frequency-specific response. For a 4.5-kHz centered NBN, DPOAE (f₂ = 4.4 kHz) inhibition was 0.1 dB (p < 0.001). This response remained present after tendon division, consistent with an MOCS origin. Low-frequency NBN (center frequency: 0.5 kHz) reduced otoacoustic emission levels (0.1 dB, p < 0.001) across a wide range of DPOAE frequencies. This low-frequency response was abolished by division of the middle ear muscle tendons, clearly indicating MEMR involvement. Conclusions: Following middle ear muscle tendon division, DPOAE inhibition by contralateral stimuli approximating the primary tone f₂ persists, whereas responses evoked by lower contralateral frequencies are abolished. This distinguishes the different roles of the MOCS (f₂ frequency specific) and MEMR (low frequency only) in contralateral modulation of DPOAE. This analysis helps clarify the pathways involved in an objective test that might have clinical benefit in the testing of neonates.

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Contralateral suppression of distortion‐product otoacoustic emissions declines with age: A comparison of findings in CBA mice with human listeners

Abstract: Functional decline of the medial olivocochlear efferent system with age precedes outer hair cell degeneration. Loss of medial olivocochlear suppressive function may play a role in the development of presbycusis in both clinical cases and animal models.

Cited by 87 publications

References 54 publications

Alpha-synuclein deficiency and efferent nerve degeneration in the mouse cochlea: A possible cause of early-onset presbycusis

Alpha-synuclein deficiency and efferent nerve degeneration in the mouse cochlea: A possible cause of early-onset presbycusis

Tinnitus with a Normal Audiogram: Physiological Evidence for Hidden Hearing Loss and Computational Model

Separating the Contributions of Olivocochlear and Middle Ear Muscle Reflexes in Modulation of Distortion Product Otoacoustic Emission Levels

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